Inactivation of GSK-3β by phosphorylation at Ser9 induced by bacterial infections results in the degradation of β-catenin, the phosphorylation of IκB by the IKK complex, freeing NF-κB to translocate to the nucleus (53), which, in turn, leads to an increase expression of pro-inflammatory cytokine genes and release of antimicrobial factors. This evidence concerns the gene NFKB1 and bacterial infectious disease.